What you're feeling¶
Charcot neuroarthropathy affects people who have lost some feeling in their feet, most often from diabetes. Because the joints cannot feel strain the way they should, walking and standing can quietly damage them. The joint becomes swollen, warm and red, and the foot may start to change shape. Many people notice little pain at first, which is part of what makes this condition easy to miss.
When there is discomfort, it usually sits in the middle of the foot or the ankle. It often flares after time on your feet, and it can be worse at night or when you first get up. Rest tends to settle it, but the swelling can take a while to go down. As the foot changes shape, everyday tasks become harder: shoes may rub or no longer fit, standing at the bench to cook becomes tiring, and walking to the letterbox or the shops can feel unsteady. Some people develop a rocker-bottom shape to the foot, where the arch has flattened and collapsed, and pressure points can break down into ulcers on the sole.
Your surgeon works out what is going on by listening to your symptoms and examining your foot, then matching what you feel with what they find. If your story and the examination do not line up neatly, further scans such as a CT or MRI can help sort out the cause. The bones in an affected foot can also become thinner, which raises the risk of small breaks happening in the joint itself.
If you have diabetes and notice a hot, swollen foot with little or no pain, it is worth having it checked promptly. Getting the diagnosis early gives your foot the best chance of staying stable.
What's actually happening¶
Charcot neuroarthropathy happens when a joint loses the protection that feeling normally provides. Healthy joints send warning signals when they are being overloaded, so you rest, change your shoes or take weight off the sore spot. When those signals are missing, the joint keeps taking the load. Small injuries pile up, and the bone starts to break down and change shape.
Two things seem to be going on inside the joint. One is wear and tear without the usual warning system: because you cannot feel the strain, you keep walking on a joint that a person with normal sensation would have rested. The other is changes in blood flow within the bone, which can weaken it from the inside. In an active Charcot foot, the cells that break down old bone become more active while the cells that build new bone do not keep up. The bone becomes thinner and weaker, which is why small breaks can happen in the joint itself.
The joints most often affected are in the middle of the foot and the ankle, where the bones and ligaments normally hold everything in a stable frame. Ligaments are strong bands that connect bone to bone and keep the joint lined up as you walk. As the bone softens and the ligaments stretch, that frame starts to give way. The arch can flatten and collapse into the rocker-bottom shape described earlier, and the joints can slip out of line. Because there is little or no pain to warn you, the damage can build up quietly until the foot changes shape or the skin breaks down.
No one fully understands why this happens, and it is likely that more than one mechanism is at work. What matters for you is the practical point: a joint that cannot feel damage cannot protect itself, so the swelling, warmth and change in shape you notice are the signs of a joint that has been quietly overloaded.
What we can do about it¶
The first step is taking weight off the affected joints so they stop being overloaded. We may suggest changes to your activity, and orthotics, which are devices worn in or on your shoes to support and protect the foot. Orthotic devices can have a real effect on how well your foot works day to day. Physiotherapy aims to keep you moving safely while protecting the joints that have lost their warning signals. We give this approach a fair trial before talking about anything further.
Pain relief and anti-inflammatory medicine can help settle the discomfort in the short term. We use these alongside the steps above, not instead of them.
If these measures have not given enough improvement, we may discuss surgery. The main option is arthrodesis, which means joining the affected bones together so the foot or ankle is stable and holds its shape during weight-bearing. A stable, flat-on-the-ground foot greatly reduces the chance of ulcers and infections coming back on the sole. In some cases we use a rod placed down through the ankle into the heel to hold the bones in place while they join. Where extra support is needed, we can add bone graft, which is bone taken from your own body to help the bones heal together. Surgery is a shared decision, and we will talk through whether it suits your foot and your goals.
What to expect¶
Charcot neuroarthropathy is a long-term condition. The swelling and warmth in an active foot usually settle over weeks to months, especially once weight is taken off the joint. But the changes to the shape of the foot tend to stay. Without treatment, the joint keeps taking load it cannot feel, and the damage builds quietly until the foot becomes unstable or the skin breaks down into ulcers.
With well-managed care, many feet stay stable and usable. Orthotics and other non-operative steps can make a real difference to how your foot works day to day. If surgery is needed, joining the affected bones together gives a stable foot in most cases, with the bones joining successfully in more than 80% of hindfoot reconstructions. Overall, surgery to correct severe deformity results in stability in 93% of patients. Most people who have this kind of surgery report better pain relief and better function, and are satisfied with the result for years afterwards.
It is honest to say that surgery on a foot with lost feeling is demanding. The bones sometimes fail to join, and infection or wound problems can happen, particularly in people with diabetes, poor circulation to the skin, or those who smoke. Careful selection matters, and surgery is generally a salvage option for feet that have not settled with other measures. In a small number of cases, saving the limb is not possible and amputation is discussed instead.
What you can realistically expect is this: with early diagnosis, protection from overload, and a team approach, most feet can be kept stable and comfortable. The sooner the condition is picked up, the more shape and function your foot keeps.
When to see someone¶
With Charcot neuroarthropathy, the warning signs are not the usual ones. A hot, swollen, red foot with little or no pain is the sign that matters, and it needs checking promptly rather than waiting to see if it settles. This matters even more if you have diabetes, because a foot that has lost feeling cannot warn you about damage the way it should. Ask for a specialist review if a foot ulcer is not healing, if the shape of your foot is changing, or if you notice new numbness or pins and needles in your feet. Go to an emergency department if your foot becomes suddenly very painful, badly swollen, or the skin breaks down with spreading redness, because these can mean a problem that needs same-day care.
Evidence & references
This is the clinical evidence summary written for health professionals. It is technical, and it lists the research this page was built from. You do not need to read it to understand your treatment or to make a decision about it.
Anatomy & Pathophysiology¶
Bony Anatomy¶
- The ankle mortise is formed by the tibial plafond, medial malleolus, and lateral malleolus [3].
- The ankle mortise articulates with the dome of the talar body [3].
- The talar dome is wider anteriorly and narrower posteriorly [3].
- The ankle mortise widens 1 to 1.5 mm during motion from plantar flexion to dorsiflexion [3].
- Medial and superior clear spaces appear wider with the foot in plantar flexion [3].
- The distal fibula has a convex medial surface that articulates with the concave incisura fibularis of the distal lateral tibia [3].
- The fibula rotates approximately 2 degrees within the incisura during ankle motion and ambulation [3].
- Ankle dorsiflexion results in external rotation and proximal translation of the fibula [3].
- The primary functions of the foot and ankle are to provide weight-bearing support and forward ambulation [3].
Ligamentous Anatomy¶
- The lateral ankle ligaments function as restraints to varus and inversion forces at the ankle [3].
- The anterior talofibular ligament (ATFL) originates from the anteroinferior aspect of the lateral malleolus, 1 cm proximal to its tip, and extends to the lateral aspect of the talar neck [3].
- The calcaneofibular ligament (CFL) extends from the tip of the lateral malleolus to the lateral aspect of the calcaneus [3].
- The posterior talofibular ligament (PTFL) extends from the posterior lateral malleolus to the posterolateral talus [3].
- The ATFL is the weakest ankle ligament [3].
- The PTFL is the strongest ankle ligament [3].
- The distal tibiofibular joint (ankle syndesmosis) and fibula provide stability against lateral talar translation [3].
- The deltoid ligament complex is the primary ankle stabilizer during stance [3].
- The deep deltoid ligament extends from the apex of the medial malleolus to the medial talar body [3].
- The deep deltoid ligament functions primarily to resist lateral talar translation and external rotation [3].
- The posterior deep deltoid is the most important component of the deep deltoid ligament [3].
- The superficial deltoid ligament extends from the distal medial malleolus to the navicular bone, sustentaculum tali of the calcaneus, medial talus, and spring ligament [3].
- The superficial deltoid ligament functions primarily to resist valgus and eversion ankle forces [3].
- The deltoid ligament consists of superficial and deep layers, with at most six bands, of which only three are constant: the tibionavicular ligament, tibiospring ligament, and deep posterior tibiotalar ligament [8].
- The superficial layer of the deltoid ligament originates from the anterior malleolus and inserts into the navicular, neck of the talus, sustentaculum tali, and posteromedial talar tubercle [8].
- The tibiocalcaneal portion of the superficial deltoid ligament is the strongest component and resists eversion of the calcaneus [8].
- The deep portion of the deltoid ligament is organized into two short, thick, discrete bands: the anterior and posterior deep tibiotalar ligaments [8].
- The anterior and posterior deep tibiotalar ligaments are intra-articular but extrasynovial [8].
- The deep posterior band comprises the largest band of the deltoid complex [8].
- The anterior deep tibiotalar ligament arises from the anterior malleolus and attaches to the medial aspect of the talus [8].
- The posterior deep tibiotalar ligament originates from the posterior malleolus and inserts on the medial body of the talus [8].
- The deltoid ligament has a rich vascular supply from three extraosseous sources: the medial tarsal artery, posterior tibial artery, and tibialis anterior artery [8].
- The deltoid ligament also has an intraosseous vascular supply from either the talus or the medial malleolus [8].
- The deep deltoid ligament has the highest load to failure at 713.8 N ± 69.3 compared with the lateral collateral ligaments [8].
- The dominant mode of failure for the deep deltoid ligament is an intrasubstance rupture near its talar insertion [8].
- The dominant mode of failure for the superficial deltoid ligament is at its insertion on the anterior malleolus [8].
Biomechanics¶
- The ankle joint is responsible for most sagittal plane motion of the foot and ankle [3].
- Ankle plantar flexion ranges from 23 to 48 degrees [3].
- Ankle dorsiflexion ranges from 10 to 23 degrees [3].
- The ankle joint also contributes to inversion, eversion, and rotation [3].
- A simplified model of the ankle joint has a horizontal axis from anteromedial to posterolateral [3].
- A simplified model of the ankle joint has a coronal axis from superomedial directed distally and laterally to the tip of the fibula [3].
- The deltoid ligament, specifically the tibiocalcaneal ligament, primarily prohibits eversion and abduction [8].
- The deep deltoid ligament, primarily the deep posterior tibiotalar ligament, resists external rotation when the foot is dorsiflexed [8].
- The deep deltoid ligament is responsible for the greatest restraint against lateral translation [8].
- Valgus tilting of the talus within the mortise requires complete rupture of both the superficial and deep deltoid ligaments [8].
Neurovascular Anatomy¶
- The superficial peroneal nerve penetrates the deep fascia and lies subcutaneously 8 to 10 cm proximal to the tip of the lateral malleolus, anterior to the subcutaneous border of the fibula shaft [6].
- The deep peroneal nerve accompanies the anterior tibial artery between the tendons of the anterior tibial and extensor digitorum longus muscles [6].
- The deep peroneal nerve lies just lateral to the anterior tibial artery and just lateral to the extensor hallucis longus tendon [6].
- The saphenous nerve is located just medial or posterior to the saphenous vein in a slightly deeper plane, 3 to 5 cm proximal to the tip of the medial malleolus [6].
- The anterior tibial artery can usually be palpated beneath the superior extensor retinaculum 4 to 5 cm proximal to the distal articular surface of the tibia [6].
- The peroneal tendons and superficial peroneal nerve are at the highest risk during intramedullary nailing of distal fibular fractures [11].
- An accessory incision for arthroscopic repair of the lateral ligament should not surpass 22 mm distance from the lateral malleolus in the anterior direction to avoid damaging the superficial peroneal nerve [11].
Fracture Classification¶
- The Danis–Weber Type A classification describes a transverse fracture of the fibula below the tibiofibular syndesmosis, sometimes associated with an oblique or vertical fracture of the medial malleolus [7].
- The Danis–Weber Type B classification describes an oblique fracture of the fibula in the sagittal plane at the level of the syndesmosis, often accompanied by an avulsion injury on the medial side [7].
- The Danis–Weber Type C classification describes a fracture above the level of the syndesmosis, indicating that the tibiofibular ligament and part of the interosseous membrane must have been torn [7].
- To achieve a reduced ankle, the fibula must be restored to its full length [7].
- To achieve a reduced ankle, the talus must sit squarely in the mortise with no tilt [7].
- To achieve a reduced ankle, the medial joint space must be restored to its normal width [7].
- To achieve a reduced ankle, there must be no tibiofibular diastasis [7].
Investigations¶
General Imaging Principles¶
- Advanced imaging is often helpful in diagnosis when combined with a thorough clinical examination [15].
- MRI is sensitive for all osteochondral lesions of the ankle, but the edema pattern frequently overestimates the severity of injury [12, 13].
- Linear fluid signal deep to subchondral bone on MRI indicates an unstable osteochondral injury [12, 13].
- MRI has a sensitivity of 92% for predicting stable versus unstable osteochondral lesions [12, 13].
Osteochondral Lesions¶
- Osteochondral lesions are seen in up to 70% of ankle sprains and 75% of ankle fractures [12, 13].
- The most common location for osteochondral lesions is the medial talar dome [12, 13].
- Modern data prove that the most common location for medial talar dome osteochondral lesions is central [12, 13].
- Medial talar dome osteochondral lesions are larger and deeper than lateral lesions [12, 13].
- The most common location for lateral talar dome osteochondral lesions is central [12, 13].
- Lateral talar dome osteochondral lesions are more often unstable, displaced, or symptomatic than medial lesions [12, 13].
- AP, mortise, and lateral weight-bearing ankle x-rays may not demonstrate subtle osteochondral lesions [12, 13].
- CT scan is helpful for determining the integrity of subchondral bone and identifying cysts in osteochondral lesions [12, 13].
Ankle Fractures and Syndesmosis¶
- MRI lacks additional diagnostic value for stability assessment of the ankle mortise in supination-external rotation-type ankle fractures [16].
- Preoperative computed tomography scans are used in operative planning for malleolar ankle fractures [16].
- Malreduction of the posterior malleolus is significantly more likely to lead to malreduction of the syndesmosis [16].
Ligamentous and Soft Tissue Pathology¶
- MRI is used for the evaluation of posterior tibial tendon dysfunction with relevance to clinical staging [1].
- MRI is used for the evaluation of anterolateral soft tissue impingement of the ankle [1, 17].
- MRI is used for the evaluation of osteochondral lesions of the talus [1].
- MRI is used for the diagnosis of ligamentous and chondral pathology in the ankle [1].
- MRI and stress radiography are used in the evaluation of chronic lateral ankle instability [1].
- MRI is used for pre-operative evaluation of the anterior talofibular ligament in chronic ankle instability [1].
- MRI findings are associated with symptoms in patients with chronic ankle sprain [1].
- MRI is used for the imaging evaluation of traumatic ligamentous injuries of the ankle and foot [1].
- MRI is used for the musculotendinous imaging of the ankle [1].
- CT and MR imaging are used for the evaluation of the postoperative ankle and foot [1].
- MRI is used for the diagnosis of plantar plate injury with reference to intraoperative findings [1].
- MRI is compared to physical examination for the diagnosis of syndesmotic injury after lateral ankle sprain [2].
- Peroneal tendon abnormalities are identified on routine magnetic resonance imaging of the foot and ankle [14].
Entrapment Neuropathies¶
- MR imaging is used for the evaluation of entrapment neuropathies of the lower extremity, including the knee, leg, ankle, and foot [18].
- Point-of-care ultrasonography is used in the diagnosis and management of superficial peroneal nerve entrapment [18].
References¶
[1] Campbell S Operative Orthopaedics 4 Volume Set. REFERENCES > FOOT AND ANKLE.
[2] Campbell S Operative Orthopaedics 4 Volume Set. REPAIR OF ACUTE RUPTURE OF LATERAL LIGAMENTS > ACUTE ANKLE LIGAMENT INJURIES, CHRONIC ANKLE INSTABILITY.
[3] Miller S Review Of Orthopaedics. SECTION 16 PATELLAR TRACKING IN TOTAL KNEE ARTHROPLASTY > BIOMECHANICS OF THE FOOT AND ANKLE.
[6] Campbell S Operative Orthopaedics 4 Volume Set. MULTIPLE Z-PLASTY RELEASE OF A CONGENITAL RING > ANKLE BLOCK.
[7] Apley And Solomon S Concise System Of Orthopaedics And Trauma. Treatment.
[8] Orthopaedic Knowledge Update Sports Medicine 6. Ankle and Foot Injuries and Other Disorders > Ankle Sprains > Medial Ankle Injury.
[11] Orthopaedic Knowledge Update 13 Ebook Without Multimedia. Foot and Ankle Anatomy and Biomechanics > Annotated References.
[12] Miller S Review Of Orthopaedics. SECTION 16 PATELLAR TRACKING IN TOTAL KNEE ARTHROPLASTY > OSTEOCHONDRAL LESIONS.
[13] Miller S Review Of Orthopaedics. OSTEOCHONDRAL LESIONS.
[14] Campbell S Operative Orthopaedics 4 Volume Set. MULTIPLE Z-PLASTY RELEASE OF A CONGENITAL RING > PERONEAL TENDONS.
[15] Orthopaedic Knowledge Update Sports Medicine 6. Ankle and Foot Injuries and Other Disorders > Summary.
[16] Orthopaedic Knowledge Update Trauma. Ankle Fractures > Annotated References.
[17] Campbell S Operative Orthopaedics 4 Volume Set. ARTHROSCOPIC EXAMINATION AND DEBRIDEMENT OF THE ANKLE JOINT > IMPINGEMENT.
[18] Campbell S Operative Orthopaedics 4 Volume Set. COMBINED HAMMER TOE AND MALLET TOE DEFORMITY WITH ASSOCIATED DOUBLE CORNS > REFERENCES > TARSAL TUNNEL SYNDROME.
